Most infections are asymptomatic or so mild as to not be recognised
and clinically recorded. In cases with overt clinical disease two main syndromes are
recognised, West Nile Fever and West Nile Virus Encephalitis. Pancreatitis, hepatitis and
myocarditis associated with WNV infection have also been described.
Acute flaccid paralysis is notable in some individuals. The main signs noted
may vary between outbreaks. (J84.5.w2,
J84.9.w13, J98.358.w2,
J101.64.w1,
J123.31.w1,
J129.42.w1,
B241.49.w49,
B242.w1,
B243.31.w1, P39.4.w3)

Patients may present with abrupt onset fever, convulsions and other signs of central
nervous system involvement. More typically, non-specific symptoms such as fever, abdominal
pain, vertigo, sore throat and respiratory symptoms progress quickly to headache,
meningeal signs, photophobia and vomiting. Lethargy, somnolence and intelligence deficits
may indicate involvement of deeper structures while more severely affected patients will
be obviously disoriented and may be comatose. Common signs include tremors, loss of
abdominal reflexes, cranial nerve palsies, hemiparesis, monoparesis, difficulties
swallowing and frontal lobe signs. Convulsions and focal signs may be present early in the
course of the disease or develop later. (B251.198.w198)

Acute, painless asymmetric flaccid paralysis of one or more
limbs, sometimes monoplegia, no numbness, paraesthesia or
sensory loss, although occasionally myalgia, often with bowel
and/or bladder involvement, often with concurrent
encephalopathy. (J84.9.w13,
J84.9.w13)

Rash has been a common finding in many outbreaks of West Nile Fever and has been
described as a characteristic finding. J99.54.w1,J111.72.w1,
B241.49.w49,
B242.w1,
B243.31.w1)
and as the second most common finding (after fever). J129.42.w1)

In about 50% of cases of West Nile Fever ( B243.31.w1),
in 50% (P31.6.w1,
J101.64.w1)
in 87% of those less than two years old, 73% of those up to five years old, but
reducing to 25% and 20% of older children and 14% of adults. (J100.93.w1)

Malaise may be noted more frequently in adults than children. (J100.93.w1)

General tiredness and weakness commonly accompany the initial fever (J101.64.w1)
and may continue during the recovery phase. (J111.72.w1)

Generalised weakness is sometimes a prominent sign in patients with encephalitis. (J98.352.w1);
e.g. recorded in 8/19 (40% of cases) of individuals with encephalitis, meningitis or
meningoencephalitis. (J84.7.w9)

Lethargy in 24.6% and general muscle weakness in 56.9% of 188
confirmed cases in Mississippi, 2002. (P48.1.w2)

Headache and other Pain:

Severe headache is commonly noted and in many outbreaks has been considered to be
one of the main symptoms. (J84.5.w2,
J84.5.w3, J84.7.w9,
J84.7.w10,
J84.7.w32,
J91.5.w1,
J99.57.w1,
J100.93.w1,
J102.17.w1,
J103.3.w1;
J106.55.w1,
J111.72.w1,
J115.13.w4,
J123.31.w1,
J129.42.w1,
B243.31.w1)

In 80% of cases (P31.6.w1);
in 51% of cases (J91.61.w1);
seen in 78% of adults and 37% of children. (J100.93.w1);
in 57.9% of cases during an outbreak in Israel, 2000. (J84.7.w14);
in 77% of 352 individuals with acute aseptic meningitis and encephalitis in Romania in
1996. (J98.352.w1

Rarely reported in experimental infection of patients with terminal neoplasia but may
have been masked by analgesics. (J91.3.w1)

Ocular pain has been reported in many cases, sometimes with a note that it has
been associated with eye movement; it has been a common sign in some outbreaks (e.g. in
45% of cases (P31.6.w1,
J101.64.w1))
although it is generally less common than headache. (P31.6.w1,
J84.5.w3,
J91.3.w2,
J100.93.w1
J101.59.w1,
J101.64.w1,
J102.17.w1;
J111.72.w1,
J129.42.w1)

Backache or back pain may be noted as a specific symptom. (J84.5.w2,
J100.93.w1,
J101.59.w1,
J107.36.w1,
J129.42.w1,
B243.31.w1);
in one outbreak this was recorded in 40% of individuals (P31.6.w1,
J101.64.w1)

Abdominal tenderness or pain has been recorded for some patients (J91.3.w2)
and noted in variable percentage of patients during outbreaks (20% of cases) (P31.6.w1),
43% (J91.61.w1)

Arthralgia (joint pain) may be noted and has sometimes been a common finding
(e.g. in 37% of patients in one outbreak (J91.61.w1),
in 2/19 (11% of cases) in another (J84.7.w9)),
in 24.5% of 188 patients in Mississippi, 2002 (P48.1.w2),
in 15/48 (31%) patients in Ontario, Canada, 2002. (J257.168.w2).
(J84.7.w9,
J91.61.w1,
J111.72.w1, J257.168.w2, P48.1.w2)

Muscle weakness/flaccid
paralysis:

Mild encephalitis and severe myelitis, described as resembling the polio syndrome. In
one individual, 68 years old. (J105.135.w1)

Flaccid paresis of the
left lower extremity with loss of deep tendon reflexes but without any sensory changes. In
one individual, 22 years old. (J107.36.w1)

Guillain-Barré
Syndrome (acute inflammatory demyelinating
polyradiculoneuritis). Progressive weakness
including proximal and distal muscles, bilateral weakness of facial muscles, and reduced
respiration such that ventilatory support was required. In one individual 69 years old. (J106.55.w2)

Muscle weakness (3/19 cases, 16% of cases). During an outbreak in and
near New York, USA 2000. (J84.7.w9)

Acute flaccid paralysis syndrome in six individuals. One or
more limbs affected with normal sensation but hyporeflexia or
areflexia and asymmetrical weakness, sometimes flaccidity. (N7.51.w1)

Acute flaccid paralysis described in seven patients, three of
which did not have other findings suggestive of severe central
nervous system involvement. In general, acute, painless asymmetric
flaccid paralysis of one or more limbs, sometimes monoplegia, no
numbness, paraesthesia or sensory loss, although occasionally
myalgia, and often with bowel and/or bladder involvement. (J84.9.w13)

Four months after onset at least three individuals remained
unable to move the affected limbs. (P48.1.w7)

Movement disorders reported include tremor (static/kinetic),
sometimes with movement, and occasionally disabling and myoclonus,
most frequently involving the upper extremity or face. Movement
disorders have generally had onset at more than five days after the
initial symptoms. In a prospective series of patients tremor was
noted in 15 individuals (94%) and myoclonus in 10 (63%). (P39.4.w3)

Parkinsonism was noted in 11 of a prospective series of patients
(68%), with cogwheel rigidity, bradykinesia and postural
instability, but no tremor at rest. This was seen in individuals
with meningitis or encephalitis. (P39.4.w3)

Bilateral leg weakness (acute flaccid
paralysis) with fever and frontal headache. Marked decreases in
motor function of both legs, particularly the right leg, and
diminished reflexes in both legs, but intact sensation. (J281.181.w1)

A review of data from 13 patients with WNV infection found that
muscle weakness associated with this infection may vary from acute
flaccid paralysis, with or without associated fever or meningitis,
through severe muscle weakness to disabling fatigue. (J292.28.w1)

Abdominal and gastro-intestinal signs:

Gastro-intestinal signs are sometimes seen and may include nausea, vomiting, diarrhoea,
abdominal pain or discomfort, less commonly anorexia, occasionally hepatomegaly or
splenomegaly. Severe pancreatitis and hepatitis have been recorded as rare complications.
(J84.5.w2,
J91.5.w1,
J123.31.w1,
J129.42.w1,
B241.49.w49,
B243.31.w1)

One or more gastrointestinal symptom(s) or abdominal abnormalities in 11/19 cases (58%
of cases). (J84.7.w9)

Anorexia or lack of appetite recorded (J91.5.w1,
J99.57.w1);
in a small proportion of cases (J101.59.w1);
in 55% of individuals. (P31.6.w1,
J101.64.w1)

Gastrointestinal signs have occurred in children without other signs considered more
typical. (J99.54.w1)

Vomiting in 53% of 352 individuals with acute aseptic meningitis and encephalitis in
Romania in 1996. (J98.352.w1)

Gastro-intestinal disturbances, anorexia and nausea in a few patients. During an
outbreak in Israel, 1952. (J101.59.w1)

Nausea noted (J84.5.w3,
J102.17.w1,
J115.13.w4);
in a small proportion of patients (J101.59.w1);
in 25% of cases (P31.6.w1,
J101.64.w1);
in8/19 cases, 42%, (J84.7.w9);
common during an epidemic in South Africa, 1974. (J111.72.w1)

Vomiting noted (J106.55.w1,
J115.13.w4));
in 10% (P31.6.w1,
J101.64.w1); (8/19
cases, 42% of cases), (J84.7.w9);
in 31.3% of cases during an outbreak in Israel, 2000. (J84.7.w14);
seen but not common during an epidemic in South Africa, 1974. (J111.72.w1);
common in an outbreak in Volgograd region of Russia, 1999. (J84.7.w32)

Abdominal pain and/or diarrhoea in 18.5% of cases during an outbreak in Israel, 2000 (J84.7.w14).

Abdominal pain and diarrhoea both rare in outbreak in
Volgograd region of Russia, 1999.
(J84.7.w32)

Anorexia, nausea, vomiting and abdominal pain considered common signs, while diarrhoea
was less common. Abdominal pains, sometimes with diarrhoea, were noted by 19% of patients;
anorexia and nausea were common and vomiting occurred in 45% of children and 19% of
adults. (J100.93.w1)

Diarrhoea and nausea seen commonly, with vomiting and tenderness of the liver both less
common. During an epidemic in South Africa, 1974. (J111.72.w1)

Acute pancreatitis with abdominal pain and high blood and urine amylase for
several days together with more usual clinical signs of fever (38°C), macular rash and
enlarged lymph nodes reported in a 20-year-old woman in Israel, 1969. (J91.23.w1)

Until recently most outbreaks of WNV disease have involved mainly West Nile Fever, with
neurological signs indicating central nervous system involvement in only a small
percentage of affected individuals. During recent outbreaks (late 1990's onwards), a high
percentage of clinical cases have involved neurological signs.

Meningitis or meningoencephalitis usually occurs at low incidence, "amounting
probably to less than 1 in 100 clinical cases." (P31.6.w1)

Rare in young adults, e.g. 1/297 cases in soldiers, but more common in the elderly
(16/49 cases). (J99.54.w1)

Light and transitory meningeal involvement seen in only a few cases, involving "a
stiff neck and Kernig's sign." During an outbreak in Israel, 1952. (J101.59.w1)

CNS involvement may occur more frequently in adults than in children. Encephalitic
signs include a depressed sensorium (drowsiness to near coma), involuntary twitching,
convulsions, hyperactivity followed by decreased activity of tendon reflexes, cogwheel
rigidity, paresis and paralysis. (J129.42.w1)

11% of individuals "showed definite or suggestive clinical signs of diffuse
encephalitis" including "depressed sensorium, ranging from drowsiness to
near-coma; involuntary twitching of hands, and occasionally of face and legs; and
irregular variation of deep tendon reflexes, usually hyperactivity followed by diminished
activity. Cogwheel rigidity was usually observed. Paralysis or paresis occurred only once
and recovery was complete... pyramidal tract signs were observed only in the one patient
with paralysis. Cranial nerves and sensory perception were never affected."
Experimental infection in patients with terminal neoplasia (J91.3.w1)

Encephalitis, apparently mild, seen in some cases. During an epidemic in South Africa,
1974. (J111.72.w1)

Insomnia noted in some cases. During an epidemic in South Africa, 1974. (J111.72.w1)

Mild weakness of the left face accompanied by fasciculations, and flaccid paresis of the
left lower extremity with loss of deep tendon reflexes but without any sensory changes. In
one individual, 22 years old. (J107.36.w1)

Guillain-Barré
Syndrome (acute inflammatory demyelinating polyradiculoneuritis). Progressive weakness
including proximal and distal muscles, bilateral weakness of facial muscles, and reduced
respiration such that ventilatory support was required. In one individual 69 years old. (J106.55.w2)

Encephalitis in two individuals, fatal in one case. In one patient confusion,
disorientation, somnolence and aphasia, progressing to decreased responsiveness, limb
spasticity, bilateral ptosis, facial nerve paralysis, bilateral Babinski response and
requirement for mechanical ventilation. In the second individual progression: "became
stuporous with severe respiratory acidosis; mechanical ventilation was begun... The
patient remained febrile and stuporous and died on day 33 of hospitalization."(J84.7.w10)

Patients with encephalitis, some of whom had profound muscle weakness (with axonal
neuropathy by electromyelogram and requiring respiratory support). (N7.48.w1)

57.9% of cases presented with encephalitis and 15.9% with meningitis. Neurological signs
included a change in level of consciousness (46.8% of cases), confused state (39.5% of
cases), nuchal rigidity (28.7% of cases), coma (16.7% of cases) and focal neurological
signs (9.4% of cases) during an outbreak in Israel, 2000. (J84.7.w14).

Confusion (disorientation and difficulty in following
commands) in one 89-year-old man with encephalitis, slow
recovery over a period of more than one month, with
disorientation remaining at one month after onset. In
Massachusetts, USA, during 2001. (J221.346.w1)

Acute flaccid paralysis syndrome in six individuals. One or
more limbs affected with normal sensation but hyporeflexia or
areflexia and asymmetrical weakness, sometimes flaccidity. (N7.51.w1)

In Ontario, Canada in 2002, a decreased level of consciousness
was noted in 75% of patients, neuromuscular weakness in 41%,
dysphagia in 34%, ataxia in 31%, dysarthria in 17%, vertigo in
14%, intention tremor in 13%, diplopia or ophthalmoplegi in 13%,
facial weakness in 11%, blurred vision in 9%, dysdiadokinesis in
8%, seizure in 6%, incontinence in 5%, tongue weakness in 5%,
myelopathy in 3%, nystagmus in 3%, Parkinsonism in 3%. (J257.168.w2)

Acute flaccid paralysis described in seven patients, three of
which did not have other findings suggestive of severe central
nervous system involvement. In general, acute, painless asymmetric
flaccid paralysis of one or more limbs, sometimes monoplegia, no
numbness, paraesthesia or sensory loss, although occasionally
myalgia, and often with bowel and/or bladder involvement. (J84.9.w13)

Four months after onset at least three individuals remained
unable to move the affected limbs. (P48.1.w7)

Movement disorders reported include tremor (static/kinetic),
sometimes with movement, and occasionally disabling and myoclonus,
most frequently involving the upper extremity or face. Movement
disorders have generally had onset at more than five days after the
initial symptoms. In a prospective series of patients tremor was
noted in 15 individuals (94%) and myoclonus in 10 (63%). (P39.4.w3)

Parkinsonism was noted in 11 of a prospective series of patients
(68%), with cogwheel rigidity, bradykinesia and postural
instability, but no tremor at rest. This was seen in individuals
with meningitis or encephalitis. (P39.4.w3)

Bilateral leg weakness (acute flaccid
paralysis) with fever and frontal headache. Marked decreases in
motor function of both legs, particularly the right leg, and
diminished reflexes in both legs, but intact sensation. (J281.181.w1)

Conjunctivitis rarely noted in the outbreak in the Volgograd region of Russia, 1999 (J84.7.w32)

Photophobia in one individual (J102.17.w1);
in 6/19 cases (32% of cases). (J84.7.w9)

Signs of papillitis (hyperemia and blurring of the disc margins) in one individual. (J102.17.w1)

Temporarily decreased visual acuity and
development of multiple round, cream-coloured chorioretinal
lesions, 300-1000µm diameter, scattered in the fundus and
persisting for over one year, together with a mild vitritis
which cleared after several months, associated with WNV
encephalitis (malaise, muscle weakness, dysarthria and
gastroenteritis) in an 81-year-old man with long-standing
nonproliferative diabetic retinopathy. In a patient in the USA,
2002.(J276.23.w1)

Clinical signs of ocular pain and
blurred vision affecting one eye, associated with fever,
headache, diffuse muscle pain and neck stiffness (WNV
meningitis). Ophthalmic examination revealed a swollen slightly
pale disc on the clinically affected side and lesser swelling on
the other side; optic neuritis was diagnosed. In a young adult
in Israel, 2000. (J277.31.w1)

Clinical signs of "floaters" in the left eye together with fatigue, left-sided frontal
headache and low-grade fever. Anterior
uveitis, vitritis and nonnecrotising chorioretinitis were noted in the left eye and milder similar findings in the right eye. Anterior uveitis responded to
steroids. Ophthalmological examination showed deep, flat, creamy whitish-yellow outer choroidal lesions, 500-750 um extending superiorly in a linear radial pattern from the optic nerve head in the left eye, and less extensive faint lesions in the right eye. The lesions were actively inflammatory. A moderate vitritis was noted overlying the optic disk and superior retina of the left eye. Small intraretinal
haemorrhages, 200um diameter , were present in the right eye and similar
haemorrhages were noted associated with some of the lesions in the left eye. Fluorescein angiography revealed blocked fluorescence ad leakage from the lesions. Treatment was initiated with local (ocular) 1%
prednisolone acetate QID. The chorioretinitis healed; two weeks after
presentation there was significantly less vitritis and a decrease in
fluorescein leakage, while the lesions appeared smaller and pigmented. This was accompanied by an improvement in visual acuity (from 20/25 OD and 20/40 OS to20/30 OS.
In a 62 year old woman in Chicago, confirmed positive for WNV IgM antibodies in serum.
(J282.121.w1)

Respiratory signs:

Respiratory signs (unspecified), without more typical signs, has been noted: in
children. (J99.54.w1);
in 23% of cases (J91.61.w1).

Pharyngitis (sore throat, reddening of the throat, congestion of the throat) has been
reported in some cases/outbreaks (P31.6.w1,
J91.5.w1,
J100.93.w1
J101.59.w1,
J101.64.w1,
J111.72.w1,
J115.13.w4,
J129.42.w1,
B241.49.w49,
B243.31.w1),
in 30% of cases in one outbreak and has been described as a characteristic finding.
(B242.w1)

In one patient suggested by palpitations, stabbing sensation and pressure in the left
chest area, with palpitations and chest discomfort persisting much longer than fever, and
ECG changes indicative of myocarditis. (J99.57.w1)

In WN virus-associated acute flaccid paralysis four months after onset at least three individuals remained
unable to move the affected limbs. (P48.1.w7)

Long-term disability is occurring in some patients with
neurological disease. (J257.168.w3)

LITERATURE REPORTS:

General reviews:

Usually a febrile, influenza-like illness, commonly with headache
and fatigue, sometimes with rash, sometimes with gastro-intestinal signs and occasionally
with signs of meningitis and/or encephalitis. (J84.5.w2)

"Clinical disease in man produced by WN virus infection is usually mild."
(B241.49.w49)

"The signs and symptoms of the disease are not specific, and their percentages
seem to differ considerably in the outbreaks reported." (J84.7.w14)
"Generally, the signs, symptoms, laboratory findings, and imaging results in WN
fever are nonspecific."(J84.7.w14)

From endemic disease in Egypt and epidemics in Israel: "a rapid onset of fever,
38-40°C, lasting for 5 to 6 days. Malaise, frontal headache, pain associated with eye
movement, and muscle pain are common symptoms. Some patients had gastrointestinal
disturbances and a sore or congested throat. Prominent signs included enlargement of lymph
nodes and a maculopapular rash. Convalescence frequently was prolonged, lasting 1 to 2
weeks." Meningeal involvement or meningoencephalitis were reported less commonly
and more frequently in older patients. (B241.49.w49)

Signs and symptoms seen vary both within and between outbreaks. (J101.64.w1)

"The incubation period is 5 to 15 days. The vast majority of infections are
asymptomatic. Mild, nonspecific symptoms include fever, headache, myalgias, rash,
conjunctivitis, and lymphadenopathy. In more serious cases, pancreatitis, myocarditis, and
hepatitis have been reported. Treatment is currently nonspecific and supportive.
Fatalities generally occur in older people, although child fatalities have been
documented." (J123.31.w1)

"The typical case is quite mild, characterized by fever, headache, backache,
generalized myalgia, and anorexia. The course of fever may be biphasic. Rash occurs in
approximately half of the cases; onset of rash is either during the febrile phase or at
the end of it. The rash is roseolar or maculopapular, is nonirritating, and principally
involves the chest, back, and upper extremities. Rash may persist for up to a week and
resolves without desquamation. Generalized lymphadenopathy is a common finding.
Pharyngitis and gastrointestinal symptoms (nausea, vomiting, diarrhoea, abdominal pain)
may occur. (B243.31.w1)
Neurological presentations include meningitis or meningoencephalitis in a small proportion
of patients (particularly elderly individuals), anterior myelitis and
encephalopolyradiculitis. Other, rare, complications include myocarditis, pancreatitis and
hepatitis. (B243.31.w1)

Fever, 101° to 105°F,
usually lasting for two or three days, but ranging from one to 12 days and in about 10% of
cases biphasic with one to two days of no fever followed by a second period of fever and
other signs. Rash is the second most common signs and is seen most frequently in children.
It may appear during or after the fever and lasts usually less than 24 hours but
occasionally several days. It is seen mainly on the trunk, less commonly on the face and
extremities, is bright pink, discrete, maculo-papular, non-painful, non-itching and not
followed by desquamation. In adults severe headache is a common complaint. Other common
signs and symptoms include chest and back pain, ocular pain, gastro-intestinal
disturbances (anorexia, nausea, vomiting, diarrhoea), lymphadenitis (single node or
generalised), sometimes a palpable (enlarged) spleen, injected conjunctiva and
pharyngitis (sore throat). Duration of the acute phase is usually three to five days but
sometimes up to 12 days. Convalescence in adults may last several weeks (weakness and
fatigue) but is shorter in children. CNS involvement may occur more frequently in adults
than in children. Encephalitic signs include a depressed sensorium (drowsiness to near
coma), involuntary twitching, convulsions, hyperactivity followed by decreased activity of
tendon reflexes, cogwheel rigidity, paresis and paralysis. Fatality rate may reach 8%. (J129.42.w1)

"Clinical features range from fever accompanied by
malaise, headache, myalgia, rash, lymphadenopathy, eye pain,
anorexia and vomiting lasting for 3 to 6 days, to severe
meningoencephalitis. Severe muscular weakness and flaccid paralysis have been experienced in several patients." (J257.168.w3)

Epidemics/Clinical case histories:

In an adult technician in Egypt: "Severe headache, primarily in the occipital
region, accompanied by muscular fatigue, particularly of the arms and legs, some initial
gastric discomfort, anorexia and fever of 38-39°C for several days
were the outstanding manifestations. Recovery was somewhat retarded but complete." (J91.5.w1)

In children in Egypt: "Fever of rapid onset, averaging
38.5-39°C, accompanied by gastro-intestinal disturbances, malaise, profuse sweating, a
fine papular rash (5 cases), moderate enlargement of the cervical, axillary and inguinal
lymph nodes (3 cases), and occasionally congestion of the eyes and throat. The fever
remained high for 5-6 days followed by gradual decline and a rather prolonged
convalescence. No signs of central nervous system involvement were observed. As far as is
known no deaths could be attributed to the infection and frank encephalitis in the highly
endemic area was exceedingly rare." (J91.5.w1)

In soldiers, fever, lymphadenopathy and rash, with meningoencephalitis in only 1/297
individuals. In other adults "a typical clinical course of varying intensity
including abortive, mild and severe cases" and one case complicated by
meningo-encephalitis. In children, "the disease ran a typical course, but the
symptoms and signs were rather mild. In several children there was involvement of the
intestinal or respiratory tracts without the appearance of more typical signs and symptoms
of West Nile fever" and one individual with meningo-encephalitis. In elderly
individuals, mainly fever of variable degree and duration (33/49 cases), in12 cases "a
severe course marked by neurological signs and symptoms of meningo-encephalitis"
with prompt recovery and in four cases the development of impaired consciousness, signs
and symptoms suggestive of severe brain damage, fulminating course and death. During an
outbreak in Israel in 1957. (J99.54.w1).

Acute pancreatitis with abdominal pain and high blood and urine amylase for several days
together with more usual clinical signs of fever (38°C), macular rash and enlarged lymph
nodes reported in a 20-year-old woman in Israel, 1969. (J91.23.w1)

Acute aseptic meningoencephalitis, meningitis or acute fever. Abrupt onset, fever
up to 39-40°C, asthenia, headache and vomiting were noted as clinical features but in
comparison with most previous outbreaks, the disease seen was generally more severe, with
central nervous system involvement frequently observed while rash, conjunctivitis,
abdominal pain, diarrhoea, respiratory symptoms and lymphadenopathy were rare. In
183/318 individuals sampled (58% of cases) serum contained anti-WN virus IgM at a level
indicative of acute infection, using an IgM-capture ELISA. It was estimated that the
epidemic involved 480 overt human cases. During an outbreak in Volgograd region of Russia,
1999.(J84.7.w32)

Acute aseptic meningitis and encephalitis in 352 individuals. "The onset of
illness was typically abrupt, with fever (91% of patients), acute headache (77% of cases),
neck stiffness (57% of cases), vomiting (53% of cases), chills (45% of cases), and
confusion (34% of cases). Disorientation, disturbed consciousness, and generalised
weakness were the predominant signs in patients with encephalitis; some patients had
decreased motor tone with hypotonia, and others had increased tone, hyper-reflexia, and
abnormal reflexes. Ataxia and extrapyramidal signs were recorded in 17% of patients, and
cranial-nerve palsies or seizures in smaller proportions. The illness progressed to coma
in 13% of cases, and among patients with confirmed or probable infection there were 17
deaths (fatality/case ratio 4.3% of cases), all in patients older than 50 years."
Also
confirmed infection in individuals diagnosed with acute respiratory infection, acute
febrile illness, monoparesis, cerebrovascular disease, chronic disease or no diagnosis.
During an outbreak in Romania (southeastern Romania including Bucharest) in 1996. (J98.352.w1)

"Sudden onset of disease characterised by malaise, general weakness, a chilly
sensation with fever, drowsiness, severe frontal headache, aching of the eyes when moved,
and pains mostly in the chest and lumbar regions. The fever rose quickly and usually
ranged between 38°C and 40°C. A small number of patients had gastrointestinal
disturbances, anorexia, nausea, and dryness in the throat. One of the characteristics was
a flushed face and injected conjunctivae." High temperatures usually remained for
two to three days before gradually returning to normal over the following three days.
General enlargement of one or more lymph nodes was a prominent finding and the spleen was
sometimes enlarged. A slight redness of the throat was noted in some individuals and a
maculopapular rash of short duration, spreading mostly over the trunk, was present in many
patients. "In very few cases light transitory meningeal involvement (a stiff neck
and Kernig's sign) was encountered during the acute stage." During an outbreak in
Israel, 1952. (J101.59.w1)

Typically fever, together with lymphoglandular swelling and/or rash. Sometimes only
lymph node enlargement or only fever. Typically (75% of cases) acute onset, almost always
with general tiredness and weakness accompanying the initial fever (38-40°C). Illness was
often moderate but in some individuals there was "great prostration and apathy."
Signs and symptoms included: fever (100% of cases), headache (80% of cases), backache (40%
of cases), chills (35% of cases), muscle pains (25% of cases), ocular pain (45% of cases),
lack of appetite (55% of cases), nausea (25% of cases), vomiting (10% of cases), abdominal
pain (20% of cases), diarrhoea (30% of cases), sore throat (30% of cases), cough (8% of
cases), flushed face (55% of cases), conjunctival injection (60% of cases), coating of
tongue (50% of cases), injection of throat (40% of cases), glandular swelling (occipital
region 75%, axillary region 90% of cases), inguinal region 85% of cases), rash (50% of
cases), spleen enlargement (20% of cases), liver enlargement (10% of cases). Rash, when
present, appeared at any time from the second to the fifth day of illness and lasted for a
period of several hours to days. Forms of rash included discrete pale roseolar spots,
diffuse small spotted pale roseolar exanthema, and mottling of the skin - pale roseolar
maculae of varying size with an indefinite border. Rash appeared most commonly on the
upper chest, back, upper arms, less commonly on the face, flanks and abdomen, and did not
appear on the lower extremities. During an outbreak in Israel, 1953. (J101.64.w1)

Fever, sore throat, headache, muscle ache, pronounced fatigue, nausea in two children
and in one of these also vomiting, flushed face, maculopapular rash and slight enlargement
of the inguinal lymph nodes; infection confirmed by a rising titre of virus neutralising
antibodies in paired serum samples (at least four-fold increase). Additionally in
other individuals with antibodies but without paired samples, in one individual severe
headache, muscle ache, pronounced fatigue, nausea, pain on eye movement, maculopapular
rash and insomnia and in two others "summer fever" with sore throat,
lymphadenitis or headache and pain on eye movement. No clinical signs had been noted in a
further eight individuals in which antibodies were detected from serum samples. In the
Czech Republic in 1999. (J84.5.w3)

Fever (86% of cases), headache (51% of cases), central nervous system involvement (46%
of cases), abdominal pain (43% of cases), arthralgia (37% of cases), respiratory signs
(23% of cases), convulsions (11% of cases) in individuals 12-40 years old. During an
outbreak in the Democratic Republic of Congo in 1998 (J91.61.w1)

Fever, headache and signs of meningismus on neurological examination in three
individuals. Additionally somnolence, skin rash and signs of papillitis (hyperemia and
blurring of the disc margins) on neurological examination in one individual, dizziness and
nausea in one individual and ocular pain, photophobia and somnolence in the third
individual. In Israel in 1980. (J102.17.w1)

In one individual, 30 years old: short term fever, headache and anorexia, together with
palpitations, stabbing sensation and pressure in the left chest area, the palpitations and
chest discomfort persisting much longer than the fever. ECG changes indicative of
myocarditis. (J99.57.w1)

In one individual, 68 years old: "mild encephalitis and severe myelitis,
resembling the "polio syndrome." (J105.135.w1)

In one individual, 22 years old. Fever, enlarged lymph nodes, mild splenomegaly,
excruciating pain in the neck, back and left lower extremity, mild weakness of the left
face accompanied by fasciculations, and flaccid paresis of the left lower extremity with
loss of deep tendon reflexes but without any sensory changes. (J107.36.w1)

In one individual 69 years old. Guillain-Barré syndrome (acute inflammatory
demyelinating polyradiculoneuritis). Progressive weakness including proximal and distal
muscles, bilateral weakness of facial muscles, and reduced respiration such that
ventilatory support was required. (J106.55.w2)

Encephalitis, meningitis or meningoencephalitis requiring hospitalisation in nineteen
individuals. "Of the 19 cases, 16(84) presented with at least one neurological
complaint (headache, stiff neck, photophobia, muscle weakness, or change in mental
status). Seventeen patients (89) had one or more abnormalities on neurological
examination. Motor exams in three patients demonstrated muscle weakness (strength
<5/5); of the six with abnormal reflexes, four were hyporeflexive, and two had abnormal
plantar responses; the two patients with cerebellar abnormalities were ataxic. Both
patients with cranial nerve abnormalities died; one had nystagmus and the other had a
depressed gag reflex. Eleven patients (58% of cases) had at least one gastrointestinal
symptom or had abnormal abdominal findings. Three patients had rash." Clinical
findings included fever (17/19, 90% of cases), fatigue (12/19, 63% of cases), altered
mental status (11/19, 58% of cases), headache (11/19, 58% of cases), weakness (8/19, 42%
of cases), nausea (8/19, 42% of cases), vomiting (8/19, 42% of cases), myalgia (6/19, 32%
of cases), photophobia (6/19, 32% of cases), abnormal reflexes (6/19, 32% of cases), stiff
neck (6/19, 32% of cases), abdominal pain (4/19, 21% of cases), cough (3/19, 16% of
cases), diarrhoea (3/19, 16% of cases), seizures (3/19, 16% of cases), arthralgia (2/19,
11% of cases), cerebellar abnormality (2/19, 11% of cases), cranial nerve palsy (2/19, 1%
of cases), shortness of breath (2/19, 11% of cases). During an outbreak in and near
New York, USA 2000. (J84.7.w9)

Encephalitis in two individuals, fatal in one case. Fever (to 39.0°C) in both
individuals, in one individual confusion, disorientation, somnolence and aphasia with
progression: "became less responsive, with limb spasticity, bilateral ptosis,
facial nerve paralysis, and bilateral Babinski response"..."mechanical
ventilation was started." In the second individual fever, chills, dizziness and
headache progressed "the patient became stuporous with severe respiratory
acidosis; mechanical ventilation was begun"... "the patient remained febrile and
stuporous and died on day 33 of hospitalization." (J84.7.w10)

Patients with encephalitis, some of whom had profound muscle weakness (with axonal
neuropathy by electromyelogram and requiring respiratory support). (N7.48.w1)

Clinical illness with encephalitis, one individual, USA, July 2001. (N7.50.w2)

Fever (39.0-40.0°C) in three children aged two, seven and ten years during a short
outbreak of disease due to West Nile virus infection in Ibadan, Nigeria in April to June
1973. (J96.72.w1)

"The main symptoms of the disease were fever, an examthem, severe headache,
sometimes accompanied by pain in back and limbs, anorexia, vomiting and abdominal pain.
Enlarged lymph nodes, angina and diarrhoea were less common symptoms."
Fever in all children and 31/37 adults, reaching 39-39.5°C, sometimes 40°C; sometimes
with chills, usually lasting two or three days, sometimes four to five days and in one
individual nine days. A second rise in temperature following one to two days of normal
temperature was seen in about 10% of cases, and was accompanied by recurrence of other
symptoms. Exanthem (bright pinkish, round discrete macules and slightly raised papules,
2-4mm diameter, often on the body and limbs, sometimes on the face, appearing during the
fever and sometimes after the fever, often lasting less than 24 hours but sometimes for
several days) present most commonly in younger individuals (87% of those less than two
years old, 73% of those up to five years old, but reducing to 25% and 20% of older
children and 14% of adults. Meningitis in ten children (as indicated by the presence of
Brudzinski's sign). Pain in the eyes, particularly on moving the eyeball, was noted by a
number of individuals. Severe headache, sometimes accompanied by "malaise
and aches in the back and limbs" was noted more frequently in adults (78% of
cases) than in children (37% of cases), although it may not have been possible to confirm
these symptoms in infants. Abdominal pains, sometimes with diarrhoea, were noted by 19% of
patients; anorexia and nausea were common and vomiting occurred in 45% of children and 19%
of adults. The throat was often slightly reddened. Severe angina was present in seven
cases. Lymph nodes were swollen and tender on pressure more commonly in adults
(submaxillary and occipital) than in children. During an outbreak in Israel (Maayan Zvi),
1951. (J100.93.w1)

Fever alone in 89%, and of no more than 1°F above baseline in 27% of these individuals.
Fever usually occurred first at 24 hours after intramuscular inoculation of virus and
persisted during the period of viraemia. A second period of fever in the third week
occurred occasionally. Headache was reported only twice but may have been masked by
analgesic agents. 11% "showed definite or suggestive clinical signs of diffuse
encephalitis" including "depressed sensorium, ranging from drowsiness to
near-coma; involuntary twitching of hands, and occasionally of face and legs; and
irregular variation of deep tendon reflexes, usually hyperactivity followed by diminished
activity. Cogwheel rigidity was usually observed. Paralysis or paresis occurred only once
and recovery was complete"... "pyramidal tract signs were observed only in the
one patient with paralysis. Cranial nerves and sensory perception were never
affected." Experimental infection in patients with terminal neoplasia. (J91.3.w1)

Signs and symptoms "frequently seen were fever, rash, muscular pain, backache,
joint pain, headache, orbital pain, diarrhoea, nausea, and those less frequently seen were
sore throat, enlarged lymph glands, vomiting, insomnia, encephalitis (apparently mild)
orchitis, enlarged and tender liver." Recovery was often "slow with
continued listlessness and weakness." No deaths were reported associated with
infection. During an epidemic in South Africa, 1974. (J111.72.w1)

Severe hepatitis associated with WNV infection (confirmed by virus isolation) in four
individuals in the Central African Republic. (B241.49.w49)

Fever for four days (about 39°C), pronounced fatigue, sore throat, headache, myalgia,
nausea, with illness lasting seven days and complete recovery after 13 days. In one
individual less than sixteen years old, infection confirmed by rising antibody titre, in
Czechland (South Moravia) 1997. (J115.13.w4)

Severe headache for two weeks, fever (39°C), general weakness and
myalgia, vomiting, confusion, blurred consciousness, signs of
meningeal irritation, photophobia. Later blurred vision, severe
vertigo, diplopia and "focal neurological signs including
right eyelid ptosis, paralysis of the right lateral rectus muscle,
flattening of the right nasolabial fold, multidirectional nystagmus,
skew deviation, excessive eye blinking (both eyes), and tongue
tremor." Neurological signs worsened, with hyperactive
reflexes, particularly on the right side, severe cerebellar ataxia
(wide based gait) and unsteadiness, and gradual worsening of visual
acuity. There was also "relative afferent pupillary defect
on the right eye, swelling of the optic discs (both eyes but more
prominent on the right eye), hemorrhages, concentric constriction of
the visual fields and a right visual field scotoma." The
patient's condition improved gradually with mild improvement first
seen after 20 days and discharge from hospital at 30 days. One case
during the outbreak of WNV infection in Israel in 2000. (J220.162.w1)

Acute fever (38.7°C), deterioration of mental status with
lethargy, disorientation and repeated generalised seizures, neck
rigidity and positive Bruzinski sign, later motor aphasia
(completely bedridden, required nasogastric feeding). Slow
improvement from the start of the third week of illness, gradual
resolution of signs (motor aphasia lasted more than three months).
One case in a four-year-old boy undergoing treatment for Hodgkin's
lymphoma during the outbreak of WNV infection in Israel in 2000. (J221.86.w1)

Fever reaching 39.4°C and confusion (disorientation and
difficulty in following commands) in one 89-year-old man with
encephalitis, slow recovery over a period of more than one month. In
Massachusetts, USA, during 2001. (J221.346.w1)

Signs in one individual of headache, myalgias, malaise, then
chills, sweats, dysesthesias, recurring hot flashes, lymphadenopathy
and anorexia, followed after two days by a maculopapular rash and
full recovery after one week. Signs in the second individual of
initial upper respiratory tract infection, accompanied one day
later by malaise, fatigue, chills and low fever (38.3°C/
100.°F); In two cases following laboratory accidents in the
USA during 2002. (N7.51.w7)

Acute flaccid paralysis syndrome in six individuals. One or more
limbs affected with normal sensation but hyporeflexia or areflexia
and asymmetrical weakness, sometimes flaccidity. Other signs varied
(e.g. fever, chills, fatigue, headache, vomiting, confusion, nuchal
rigidity etc.). During 2002 in the USA. (N7.51.w1)

Natural infection with acute flaccid paralysis in seven patients.
At initial presentation fever (at least 38.5°C) in 6/7, headache in
6/7, nuchal rigidity in 3/7, altered mental status in 3/7 and tremor
in 4/7. One or more limbs, upper and or lower limbs, affected, also
bulbar muscles in one individual. Acute flaccid paralysis without
sensory loss or paresthesias, marked asymmetric weakness, diminished
or absent deep tendon reflexes in affected limb(s). Associated with
disease of the anterior horn cells of the spinal cord. (J84.9.w13)

Acute flaccid paralysis described in seven patients, three of
which did not have other findings suggestive of severe central
nervous system involvement. In general, acute, painless asymmetric
flaccid paralysis of one or more limbs, sometimes monoplegia, no
numbness, paraesthesia or sensory loss, although occasionally
myalgia, and often with bowel and/or bladder involvement. (J84.9.w13)

Movement disorders reported include tremor (static/kinetic),
sometimes with movement, and occasionally disabling and myoclonus,
most frequently involving the upper extremity or face. Movement
disorders have generally had onset at more than five days after the
initial symptoms. In a prospective series of patients tremor was
noted in 15 individuals (94%) and myoclonus in 10 (63%). (P39.4.w3)

Parkinsonism was noted in 11 of a prospective series of patients
(68%), with cogwheel rigidity, bradykinesia and postural
instability, but no tremor at rest. This was seen in individuals
with meningitis or encephalitis. (P39.4.w3)

In India, 2002. Mainly (81/88 confirmed cases) classical West Nile
fever with fever, headache, general aches, nausea and vomiting, but
also seven cases of encephalitis. (J260.33.w1)

Temporarily decreased visual acuity and
development of multiple round, cream-coloured chorioretinal lesions,
300-1000µm diameter, scattered in the fundus and persisting for
over one year, together with a mild vitritis which cleared after
several months, associated with WNV encephalitis (malaise, muscle
weakness, dysarthria and gastroenteritis) in an 81-year-old man with
long-standing nonproliferative diabetic retinopathy. In a patient in
the USA, 2002. (J276.23.w1)

Clinical signs of ocular pain and
blurred vision affecting one eye, associated with fever,
headache, diffuse muscle pain and neck stiffness (WNV
meningitis). Ophthalmic examination revealed a swollen slightly
pale disc on the clinically affected side and lesser swelling on
the other side; optic neuritis was diagnosed. In a young adult
in Israel, 2000. (J277.31.w1)

Clinical signs of "floaters" in the left eye together with fatigue, left-sided frontal
headache and low-grade fever. Anterior
uveitis, vitritis and non-necrotising chorioretinitis were noted in the left eye and milder similar findings in the right eye. Anterior uveitis responded to
steroids. Ophthalmological examination showed deep, flat, creamy whitish-yellow outer choroidal lesions, 500-750 um extending superiorly in a linear radial pattern from the optic nerve head in the left eye, and less extensive faint lesions in the right eye. The lesions were actively inflammatory. A moderate vitritis was noted overlying the optic disk and superior retina of the left eye. Small intraretinal
haemorrhages, 200um diameter , were present in the right eye and similar
haemorrhages were noted associated with some of the lesions in the left eye. Fluorescein angiography revealed blocked fluorescence ad leakage from the lesions. Treatment was initiated with local (ocular) 1%
prednisolone acetate QID. The chorioretinitis healed; two weeks after
presentation there was significantly less vitritis and a decrease in
fluorescein leakage, while the lesions appeared smaller and pigmented. This was accompanied by an improvement in visual acuity (from 20/25 OD and 20/40 OS to20/30 OS.
In a 62 year old woman in Chicago, confirmed positive for WNV IgM antibodies in serum.
(J282.121.w1)

Fever (102.9°F/39.4°C), frontal
headache and bilateral leg weakness (acute flaccid paralysis).
Marked decreases in motor function of both legs, particularly
the right leg, and diminished reflexes in both legs, but intact
sensation. (J281.181.w1)

Infection in horses is commonly asymptomatic. However
disease characterised by neurological signs may occur, sometimes with fever reported early
in the course of the infection although fever has not been a consistent finding. Onset of
nervous signs such as ataxia
or paresis
may be acute or apparent lameness may progress to obvious
ataxia. Ataxia may progress to recumbency
with inability to rise. Clinically affected
individuals may recover, with or sometimes without supportive treatment, or severe signs
may result in death or signs of a severity requiring euthanasia. Full resolution of ataxia
in survivors may take weeks to months. (J4.218.w2,
J4.222.w1, J64.19.w1,
J84.7.w12,
J84.7.w17,
J84.7.w27,
J89.16.w1)

In fatal cases (death or euthanasia required), ascending paresis,
tetraplegia and recumbency, or early tetraplegia and recumbency, usually with muscle
rigidity and hyperreflexia of the hind limbs (6/14 horses). (J87.32.w1)

Weakness considered one of the characteristic signs, Camargue, 1962). (J84.7.w17)

Progressive weakness of the hind quarters prior to recumbency in a horse
in Egypt. (J86.57.w1)

Tetraplegia progressing from ataxia and resulting in
recumbency in one horse in Israel in 2000. (J3.151.w1)

Paresis in two, hindlimb paraplegia in one and quadriplegia in
two, from five fatal cases during an outbreak in Israel in 2000.
(J73.57.w1)

Limb ataxia or paresis, symmetrical or asymmetrical, most commonly
involving the hind limbs but occasionally only affecting the front limbs; signs may be
exacerbated by moving the animal backwards. (J89.16.w1)

Depression was recorded in 10/28 (36%) cases in Ontario,
Canada, 2002. (J14.44.w1)

Abnormal mentation was noted in 31/46 horses (67%) admitted in
Florida, 2001. These included four horses which could be roused
only with difficulty and four which showed aggression. Four
individuals circled or stall-walked compulsively. (J4.222.w1)

Lethargy or depression was noted in 43.0% (208/484) equines,
altered mentation in 22.1% (107/484), 13/484 were apprehensive and a further
eight equines were restless or agitated, in Nebraska and
Colorado, USA, 2002. (J4.225.w2)

Compulsive behaviour was noted in 6.8% (33/484) of equines in
Nebraska and Colorado, USA, 2002. (J4.225.w2)

Depression was a common finding, seen in 31.9% of horses in a
study in Texas, 2002. (J238.118.w1)

Excitability was seen in horses with severe clinical signs
requiring euthanasia in Kentucky, USA, 2002. (J305.55.w1)

Poor appetite was noted in 27.9% (135/484) of equines, 13 had ocular problems such as blindness, 7/484 had localised or
generalised oedema and 7 had abnormal
respiration, in Nebraska and Colorado, USA, 2002. (J4.225.w2)

Sweating was noted as one of the less common signs in horses in a
study in Texas, 2002 (J238.118.w1)

Following discharge from veterinary case, of 19 survivors which
could be traced, 3/19 were clinically normal at the time of
discharge, a further 5/19 within a month, 5/19 within three months
and 4/19 within six months; 2/19 had apparently not returned to
normal by six months. (J4.222.w1)

A study of 133 horses diagnosed with WNV infection in Minnesota found
that of the
125 which survived initial illness, 74 had no residual signs; the duration of
clinical abnormalities in these 74 (59.2%) completely recovered horses
ranged from one to 180 days (median 21 days, mean 35 days). However, 40% of the horses showed
either gait abnormalities, behavioural changes, or both at about six
months after the original diagnosis. Additionally, while
92 horses were considered by their owners to be "fully recovered",
only 74 had no currently observable behavioural or neurological
abnormalities: eight had behavioural changes, two had loss of
muscle mass, two showed more frequent stumbling, two had diminished
energy level, one had hind limb weakness and one an abnormal gait; eight
horses had two abnormalities including four with both behavioural
changes and gait abnormalities while one had both loss of muscle mass
and vision loss (owner observations). A further 22 horses were
owner-classified as having incomplete recovery; 17 of these had gait
abnormalities (abnormal gait, hind- and/or fore- limb weakness, or
stumbling) (owner-classifications), 15 had behavioural changes, six
showed loos of muscle mass and four had decreased energy. Two horses
were euthanased at six and seven months post diagnosis because of
persistent severe gait defects. Relapses were reported also. Behavioural
changes were described as one of three types: change in demeanour,
change in mental abilities and abnormal behaviour patterns. The results
of the survey "suggest that it will be difficult for
veterinarians to give clients a very good prognosis for full recovery
from this disease." (P51.49.w1)

A study of 482 equids (mostly horses) with clinical WNV infection in
Nebraska and Colorado in 2002 found that of 339 individuals which
survived infection, 271 (79.9%) recovered fully after a mean disease
duration of 22.3 days (+/- 18.8 days, range less than one day to 90
days). However, 20.1% (68 individuals) were reported to be still
affected at the time of the survey; in the 67 for which continuing signs
were described, they included 14 (21%) with loss of weight or body
condition, 13 (19%) with lethargy or decreased stamina, eight (12%) with
continuing ataxia, seven (10%) with stumbling, and five (7%) with
cranial nerve deficits - droopy ears, lips, muzzle. (J4.225.w2)

In 17 horses with WNV lineage 2 neuroinvasive disease in Hungary
in 2008,nine
horses recovered, five were euthanased or died due to the acute disease
and three continued to show clinical signs after six months. (J275.25.w1)

LITERATURE REPORTS:

"Neurological disease in horses is characterised principally by
posterior ataxia, proprioception deficits and altered behaviour. The most severe cases
evolve to paralysis of the hind legs, recumbency, terminal convulsion and death."
(J64.19.w1)

Case fatality rate for horses with clinical disease has been 43-45%. (J64.19.w1)

Infection rate in horses residing near to individuals showing clinical
signs may be about 20-40%. (J64.19.w1)

"WN infection in horses may cause acute, fatal neurological
disease, but clinical disease often does not occur. Moderate to severe ataxia, weakness
and rear limb incoordination were the most consistent signs; fever was not."(J84.7.w27)

In clinical cases, variable from temporary neurological deficits to
fulminating fatal encephalitis; infection does not always result in clinical disease. (J89.16.w1)

Muscle fasciculation, fever , facial paralysis, facial twitching,
grinding of teeth and blindness were all reported more commonly in affected horses in the
USA in 2000 than in 1999. (J84.7.w12)

Clinical signs:

Characterised by ataxia, weakness and amaurosis. Fatal in about 25-30% of cases. France
(Camargue), 1962. (J137.118.w1)

Clinical WNV infection was characterised by acute onset of rear limb
ataxia and included muscle tremors, knuckling over at the fetlocks, and in some instances
inability to rise. Death in 4/20 horses, full recovery in the surviving individuals.

No signs in some infected horses (20/69 asymptomatic stable mates of
clinically affected horses had positive WN virus titres). In New
York State, USA 1999. (J84.7.w27)

Ataxia in 95.7% of the 23 confirmed cases, affecting the rear limbs in
90.5% and all four limbs in 75%; acute onset in 90.5% of horses, fever greater than 101°F
(mean 102.4°F, range 101.4-103°F) in 31.8%; muscle fasciculation in 55%, almost falling
in 47.1%, recumbency in 40.9% of horses while 28.6% were able to rise with assistance;
dullness and lethargy in 26.3%; hypermetria in 25% and agitation in 15.8%; 34.8% of ill
horses died. Full eventual recovery of surviving individuals. In New York State, USA 2000.
(J84.7.w27)

Limb ataxia or paresis, symmetrical or asymmetrical, most commonly
involving the hind limbs but occasionally only affecting the front limbs; signs may be
exacerbated by moving the animal backwards. Wide-based stance, hypermetric or staggering
gait, stumbling, circling, leaning to one side, head tilt, proprioceptive deficits (seen
as toe-dragging). Behavioural changes (depression, fearfulness) sometimes observed. Ataxia
may take weeks to months to fully resolve. (J89.16.w1).

Clinical encephalomyelitis in one of 12 horses experimentally infected by mosquitoes. (J133.951.w37)

Marked gait abnormalities in all cases; with variable degrees of ataxia
and hind limb weakness, sometimes also one or both forelimbs affected.
Tremors in 4/14 horses. Recovery in 5-15 days in 8/14 horses. Ascending paresis,
tetraplegia and recumbency, or early tetraplegia and recumbency, leading to death or
euthanasia; usually with muscle rigidity and hyperreflexia of the hind limbs (6/14
horses). Traumatic lesions of the forelimbs and head in recumbent animals, associated with
compulsive movements. Italy, 1998. (J87.32.w1)

Pyrexia, lachrymation, asthenia, developing to hindquarter paresis then
hind leg paralysis, recumbency, sometimes scraping of a hole with the fore legs, and death
in 5-10 days. Morocco. (J85.108.w1)

Egypt: Colic, haematuria and urine retention reported, followed by
staggering gait, progressive weakness of the hind quarters, recumbency; death in about 60
hours after the onset of illness. (J86.57.w1)

Experimental infection with an isolate from a crow (Corvus
brachyrhynchos - American Crow). No clinical signs in 3/4
horses. Nervous signs in 1/4, beginning 58 days post-inoculation, including reluctance to
move, apprehension, proprioceptive defects and a drooping and twitching lower lip but no
fever and no loss of appetite. USA, 1999. (P32.1.w13)

Ataxia affecting the hindlimbs or all four limbs, progressing to
quadriplegia in one horse and to recumbency in that horse and some
other horses. Fever with no other signs was noted in one animal from
which virus was isolated and fever was noted in at least three other
horses which did have neurological signs. Reduced appetite was noted
in two horses, one of which also had "mild signs of colic".
Signs noted in single horses included jaundice, hyperexcitability
and tooth grinding. One horse had notable respiratory signs, with a
raised respiratory rate (40-48 per minute), inspiratory dyspnoea and
narrowed glottis due to failure to abduct the arytenoids.
In horses
in Israel in 2000. (J3.151.w1)

Israel, 2000, data from five fatal cases: ataxia progressing to
recumbency in all five horses. Paresis was noted in two animals,
paraplegia of the hind legs in two others and quadriplegia in the
fifth. Fever was noted in three horses and circling was a feature in
one of the horses. Illness lasted 2-7 days, with two animals euthanised
when recumbent at two and three days of illness. (J73.57.w1)

Canada, Sascatchewan, 2002. A nine-year-old gelding showed acute onset ataxia of all four limbs, with weakness and proprioceptive defects, also muscle fasciculation (particularly the face, upper lip, trunk and limbs, and depression, but with periods of hyperresponsiveness. Appetite remained good and the horse improved after two days. A 16-year-old
mare showed acute onset lateral recumbency, initially with normal mental state and appetite, but progressing to reduced responsiveness, thrashing, flaccid tail, tense, firm hind quarters, and reduced anal tone (rectum full of faeces); the mare
was euthanized after 24 hours.
Treatment was supportive, including provision of a deep bed, and, for treatment of uncontrolled thrashing leading to self-injury, sedation with xylazine, ketamine and
acepromazine. (J14.45.w1)

Florida, USA, 2001. Data from 46 cases of confirmed WNV infection:
fever in 30/46 (65%), anorexia in 26/46 (57%), weakness or ataxia in
46/46 (100%) (including weakness in 43/46 (94%) and ataxia in 33/46
(72%)), recumbency in 14/46% (30%), dysmetria in 18/22 evaluated
(82%), abnormal mentation in 31/46 (67%), fasciculations in 28/46
(61%, including face or neck only in 12/46 horses (26%) and the
whole body in 16/46 horses (35%), cranial nerve deficits in 20/46
(44%), seizure in 2/46 (4%), teeth grinding in 9/46 (20%) and
ptylism in 3/46 (7%). High temperature together with spinal
cord deficits was seen in 61%, high temperature and change in
mentation in 65% and high temperature together with fasciculation in
54%, but less than 30% showed three of the commonest abnormalities
in combination. Abnormalities of mentation included aggression
(4/46), periods of sudden cataplexy or narcolepsy (16/46) and
compulsive behaviour (circling or stall walking) in 4/46. The
overall mortality rate was 30% (including three horses euthanized
one to six months later for associated problems). (J4.222.w1)

A study of 133 horses diagnosed with WNV infection in Minnesota found
that of the
125 which survived initial illness, 74 had no residual signs; the duration of
clinical abnormalities in these 74 (59.2%) completely recovered horses
ranged from one to 180 days (median 21 days, mean 35 days). Of the 125
horses which had survives the acute illness, 40% of the horses showed
either gait abnormalities, behavioural changes, or both at about six
months after the original diagnosis. Of the horses in the study group,
92 were considered by their owners to be "fully recovered",
but only 74 had no currently observable behavioural or neurological
abnormalities: eight had behavioural changes, two had loss of
muscle mass, two showed more frequent stumbling, two had diminished
energy level, one had hind limb weakness and one an abnormal gait; eight
horses had two abnormalities including four with both behavioural
changes and gait abnormalities while one had both loss of muscle mass
and vision loss (owner observations). A further 22 horses were
owner-classified as having incomplete recovery; 17 of these had gait
abnormalities (abnormal gait, hind- and/or fore- limb weakness, or
stumbling) (owner-classifications), 15 had behavioural changes, six
showed loos of muscle mass and four had decreased energy. Two horses
were euthanased at six and seven months post diagnosis because of
persistent severe gait defects. Relapses were reported also. Behavioural
changes were described as one of three types: change in demeanour,
change in mental abilities and abnormal behaviour patterns. The results
of the survey "suggest that it will be difficult for
veterinarians to give clients a very good prognosis for full recovery
from this disease." (P51.49.w1)

USA (Nebraska and Colorado) in 2002. In a study of 484 affected equids from 57.4% (278/484 ) were ataxic, 53.3% (259/484) had generalised weakness, 43.0% (208/484) were lethargic or depressed, 42.6% (206/484) had muscle fasciculations, 36.6% (177/484) were stiff or reluctant to move, 27.5% (133/484) were recumbent and unable to rise, while
a further 24.2% (117/484) were recumbent for long periods but able to rise, 27.9% (135/484) had poor appetite, 22.1% (107/484) showed altered mentation, 21.1% (102/484) fever, 20.9% (101/484) were lame, 20.7% (100/484) had abnormal head carriage, 19.0% (92/484) had
cranial nerve deficits, 19.0% (92/484) had hyperaesthesia, 10.3% (50/484) used a dog-sitting posture, 8.1% (39/484) had dysphagia, 6.8% (33/484) compulsive behaviour,
6.4% (31/484) hypermetria, 6.2% (30/484) muscle atrophy, 5.0% (24/484) had seizures, 3.1% (15/484) used a praying posture, 2.7% (13/484) showed head-pressing. 13/484 were apprehensive and a further 8 were restless or agitated, 13 had ocular problems such as blindness, 7/484 had localised or
generalised oedema and 7 had abnormal respiration. (J4.225.w2)

USA (North Dakota) in 2002. A study of 569 cases found
incoordination in 69%, muscle tremors/twitches in 52%, limb weakness
or paralysis in 38%, caudal paresis in 29%, recumbency or difficulty
in rising in 23%, lip droop in 21%, tooth grinding in 8%, fever in
7%, circling in 6% and blindness in 3%. For the 471 horses in which
outcome was known, 27% died or were euthanized. (J4.225.w3)

USA (Indiana) 2002. The most common clinical signs were ataxia in
75/136 horses (44/1%), hind limb paresis in 60/136 (35.3%), muscle
tremors/fasciculations in 60/136 (35.3%), recumbency in 13/136
(7.6%); fever was not a common finding. (J4.225.w5)

Hungary, 2008. In August to October 2008, neurological disease
in 17 horses, with ataxia and weakness the most common signs. Nine
horses recovered, five were euthanased or died due to the acute disease
and three continued to show clinical signs after six months. (J275.25.w1)

Donkey:

USA (Nebraska and Colorado) in 2002. At least one affected
donkey became recumbent and was euthanized. (J4.225.w2)

Fever and encephalitis with signs such as ataxia and prostration may result following
intracranial or intranasal inoculation, but intravenous inoculation has resulted in only
fever with asymptomatic infection following subcutaneous inoculation.

Fever
and encephalitis following intracerebral or intranasal inoculation; only fever following
intravenous inoculation, and the development of immunity. (J120.20.w1)

"Very susceptible to intracerebral (i.c.) inoculation of the virus."
Viraemia, fever, ataxia and prostration following intracerebral inoculation. May be
full recovery in one to two months or sometimes prolonged severe flaccid paralysis of the
extremities. With intraperitoneal or intramuscular inoculation no clinical disease but
sometimes short term viraemia. Egypt strain, 1950. (J122.77.w1)

Fever:

Not seen following subcutaneous inoculation, but recorded developing 7-8 days
after intracerebral inoculation, including in individuals with no other clinical signs.
(J71.75.w1)

Temperature
40.0°C or higher on the fifth, sixth and eighth days after intracerebral inoculation in
one individual. Subnormal temperature recorded on the tenth day (moribund); in a second
individual fever in excess of 40.0°C was noted on the 7th and 8th days.
(J120.20.w1)

Temperature 40.0°C or higher on the seventh and eighth days in one individual and on
the fifth to eighth days of a second individual (as well as at four and 20 hours
post-inoculation in this individual). (J120.20.w1)

Encephalitis
recorded, sometimes fatal, following intracerebral inoculation of virus, starting 3-5 days
after the onset of fever in 34/56 individuals inoculated intracerebrally: (J71.75.w1)

"ataxia,
tonic and clonic convulsions, tremor of the extremities, slight decrease of the muscle
power in the upper and lower extremities (usually asymmetrical), decrease or asymmetry or
tendon reflexes." (J71.75.w1)

Signs
progressed over several days with "the appearance of ptosis, paresis of the
extremities and sphincters, adynamia, and marked hypothermia." (J71.75.w1)

Death
in 2-6 days after the onset of nervous signs or "significant regression of the
symptoms" within two weeks. (J71.75.w1)

"Reduced
muscle power in the extremities" was recorded for up to 35-36 days in some
individuals. (J71.75.w1)

Obvious
signs of encephalitis by the seventh day after intracerebral inoculation of one
individual: "tremors, spasticity, nystagmus, excitability and incoordination."
By the eighth day marked weakness and convulsions. Weakness progressed to coma; moribund
by the tenth day post-inoculation. (J120.20.w1)

Illness from the evening of the fourth days, then "rigors and progressive loss
of appetite until the 8th day, when coarse tremors, incoordination, and weakness were
seen. On the afternoon of the 9th day the animal was very ill; the temperature had fallen
and it was sacrificed." (J120.20.w1)

One individual "became hyperactive and showed rigors on the 8th day; exhibited
marked weakness, loss of appetite, and apathy on the 9th to 11th days; appeared improved
on the 12th day; and was apparently recovered by the 14th day." (J120.20.w1)

Following intravenous inoculation, no nervous signs seen in
two individuals. (J120.20.w1)

Ataxia and prostration following intracerebral inoculation of WN virus. Signs may
improve to normal by one to two months or a severe flaccid paralysis of the extremities
may remain. Egypt strain, 1950. (J122.77.w1)

Virus isolated from blood on the first day after inoculation in 1/1 individual tested
and possibly at low titre on the 2nd and 3rd days (detection by mouse inoculation test,
resulting in the deaths of 1/5 and 1/8 mice (Mus
domesticus - Laboratory mouse) respectively). (J120.20.w1)

Neutralizing antibodies detected by 19 or 25 days after intracerebral inoculation in two
individuals. (J120.20.w1)

Experimental infection resulted in viraemia and seroconversion but no clinical signs. (J91.34.w1)

LITERATURE REPORTS:

No
clinical signs recorded following inoculation with either of two strains of WN virus. (J91.34.w1)

Viraemia
detected at 1-3 days and 3-4 days post infection in two individuals inoculated with Egypt
101 strain and at day 1or 2 to 6, and on day 10, in two lemurs inoculated with MG An
798 stain (originally isolated from a parrot in Madagascar). Viraemia was sufficient to
infect mosquitoes (Aedes
aegypti), particularly following infection with the Madagascan strain of WN
virus. (J91.34.w1)

Natural infection been reported associated with clinical illness
(fever, neurological signs, death) in one individual and with head
hanging, lagging behind others, ataxia and teeth grinding, in
another individual.

With experimental infection, mild biphasic fever has been recorded and in
one case congenital deformity associated with infection of a pregnant ewe.

Fever: Mild biphasic fever following experimental infection of two 7-9
old sheep and moderate increase in body temperature two days after infection in one of two
18 month old pregnant ewes following experimental infection.(J62.53.w3)

Reproductive: Of
twins born to an experimentally infected ewe in which fever and viraemia were detected,
one lamb was clinically normal while the other was weak and dumb; this lamb
died at two days old and hydroencephaly was observed. (J62.53.w3).

Neurological signs and fever: Fever 104-106°C, hind limb
paralysis progressing to convulsions and death within two days of
the onset of clinical signs in a six-year-old Suffolk ewe in
Nebraska, 2002.(W27.16Sept02.wnv1)

Neurological signs: Diffuse muscle fasciculations and
inability to stand, progressing to lateral recumbency. Also apparent
hyperaesthesia, intermittent rigid extension of the hind limbs,
occasional but increasing tonic-clonic convulsions, distended
urinary bladder and traumatic lesions (abrasions of the facial skin,
corneal ulcer) associated with recumbency. Continued to eat and
drink, but estimated 6% dehydrated. Appeared depressed but alert and
responsive. (J275.17.w1)

Neurological signs: in a single ewe in a flock in
Hungary, 2005, lagging behind, head hanging, ataxia, grinding of
teeth. (J3.161.w2)

Neurological signs including nystagmus (horizontal), ataxia, head
tilt, lateral recumbency and death in seven goats (males and
females, 16 months to two years old). No signs in the remaining five
goats of the flock. (W27.16Sept02.wnv1)

In one alpaca in 2002, fatal infection with clinical signs of
"torticollis, ataxia, recumbency and 'crying like in pain'"
in the three and a half days of clinical illness before death. (W27.17Sept02.wnv1)

No clinical disease following experimental infection via mosquito
bite; maintenance of normal activity levels. Mild increase in body
temperature in one individual within 12 hours of infection; the
individual was in prooestrus at this time. (P39.4.w16,
J84.10.w1)

Natural infection reported in four dogs,
age five months to six years, with fever and neurological signs; three
of the dogs died. WNV infection confirmed by the presence of WN virus
neutralising antibodies but the virus was not confirmed to be the cause
of the illness. In Louisiana, USA, 2002. (W27.18Oct.wnv1,
W27.24Oct02.wnv1)

In one individual, inability to bear weight
on its limbs even while being supported, conscious deficits in
proprioception of the pelvic limbs, altered mentation and pyrexia
(40.3°C). Infection confirmed serologically in a further four dogs
without related clinical signs. (J212.15.w3)

Lethargy, modest reduction in appetite and mild increase in
rectal temperature recorded in some cats following experimental
infection by mosquito bite; seizures reported in a single
naturally infected individual. (J64.19.w1,
P39.4.w16,
J84.10.w1)

LITERATURE REPORTS:

Seizures reported in a single cat. Euthanised. Infection confirmed by isolation of West Nile virus from the brain. (J64.19.w1)

Mild non-specific clinical signs lasting two
to three days and increased rectal temperature for days 1-6 after
infection in cats experimentally infected via mosquito bite. (P39.4.w16)

Flu-like illness for one to two days following experimental
infection. (P48.1.w16)

Lethargy, modest reduction in appetite and fluctuating febrile
response in three of four cats infected by bite of infected
mosquitoes but not in any of four cats infected by ingestion of
infected mice. (J84.10.w1)

Hind limb paresis/paralysis was noted in a male polar bear. He was unable to stand, with a weak left hind leg and inability to move the right hind leg. The bear appeared depressed and also developed more pronounced breathing.
(V.w114)

Adult mice, infection by intracerebral inoculation. Death or illness and sacrifice of
9/10 mice inoculated initially. Subsequently (mouse-to-mouse intracerebral passage of
infected mouse brain in saline)100% fatality. Initial inoculation illness by six to eight
days post-inoculation. First passage incubation period six days, second and third passages
incubation period four days, later three days, sometimes with detectable illness at two
days. Longer incubation period if a lower dose of virus was inoculated (incubation period
4-5 days and survival time 5-10 days). (J120.20.w1)

"Illness appeared 3 days after inoculation and was manifested by sequential
development of the following signs: hyperirritability, failure to feed, falling on back
and inability to get up, tremors, stupor, coma and death." In suckling mice
inoculated intracerebrally with 100 host LD50 of Egypt 101 strain.(J101.86.w2)

Mild clinical signs by day six following intraperitoneal inoculation in one mouse,
neurological signs including ataxia, weakness and bilateral limb paralysis days 7-9 in two
mice, severe illness by day eight in one mouse (sacrificed on day eight), ruffled fur at
day eight and death by day nine in one mouse. Also up to 9% weight loss. (J133.951.w12)

The results of infection appear to be age dependent, with fatal infection following
either intracerebral or intraperitoneal inoculation of newborn rats, encephalitic signs
(e.g. sluggishness, hyperirritability) in animals inoculated intracerebrally at 16 days
old but no clinical signs following inoculation of animals at even two months old.
(J100.93.w1,
J101.86.w2,
J116.5.w1)

LITERATURE REPORTS:

Two months old rats. Intracerebral or intraperitoneal inoculation, no signs. WN
virus strain isolated from a rook (Corvus
frugilegus - Rook) in the Ukraine, 1980. (J116.5.w1)

No clinical signs following intracerebral inoculation. During an outbreak in Israel
(Maayan Zvi), 1951. (J100.93.w1)

"Encephalitic signs such as sluggishness and hyperirritability on days 4 and 5
after inoculation, but all recovered." In sixteen day old rats following
intracerebral inoculation of Egypt 101 strain. (J101.86.w2)

"Signs of encephalitis appeared 2 to 8 days after intracerebral inoculation,
depending on the virus dose and on the host [age and species i.e. rat or mouse]".
(J101.86.w2)

Newborn rats (less than six hours old) were highly susceptible to intracerebral or
intraperitoneal inoculation with WN virus, with fatal infection. (J101.86.w2)

Generally no clinical signs following infection with a variety of WN virus strains, even
after intracerebral inoculation. A temperature rise for one day in one animal has been
recorded following intracerebral inoculation. Viraemia may be detected and high titres of
antibodies develop. (J100.93.w1,
J101.59.w1,
J116.5.w1,
J120.20.w1,
J122.77.w1).

No
clinical signs following very high dose intracerebral inoculation. Seroconversion occurs.
(J101.59.w1)

No
clinical signs following intracerebral, intranasal or intraperitoneal inoculation of
adults nor in 150g juveniles. (J120.20.w1)

One day rise in body temperature in one individual, otherwise no clinical signs
following intracerebral inoculation. Circulating virus demonstrated (by mouse inoculation)
on the second day post-inoculation. High level of complement-fixing antibodies developed.
During an outbreak in Israel (Maayan Zvi), 1951. (J100.93.w1)

No clinical signs following intracerebral inoculation but development of high titre
antibodies. Egypt strain, 1950 (J122.77.w1)

"Various signs of neurological disease including weakness,
depression, head tilt, torticollis, lateral recumbency,
uncoordinated movements, inability to right themselves when pushed
over, and scratching of their foreheads with both feet and tremors."
In two juveniles. (J26.40.w1)

Experimental inoculation by a variety of routes commonly produces clinical disease with
nervous signs such as hind limb paralysis, tremors, difficulty in walking, tremors, loss
of balance prior to death in fatal cases. Residual nervous signs may be seen in survivors.
Susceptibility is highest following intracerebral inoculation, lower with intraperitoneal
or subcutaneous inoculation. (J84.7.w20,
J91.65S3.w2,
J100.93.w1
J101.59.w1)

Lethargy and huddling together may be seen, e.g. 6-7 days after intraperitoneal
inoculation. (J84.7.w20)

Reduced feeding, drinking and grooming may be seen, e.g. 6-7 days after intraperitoneal
inoculation. (J84.7.w20)

Recovery and Convalescence:

.Residual nervous signs including tremors, muscle weakness and difficulty in walking may
be seen in animals surviving clinical disease. (J84.7.w20)

LITERATURE REPORTS:

One-month-old hamsters. Intracerebral inoculation of
strains from humans in Israel resulted in death of all hamsters, frequently with signs of
encephalitis prior to death (death within 12-24 hours of clinical symptoms). Lower
susceptibility following intraperitoneal or subcutaneous inoculation. (J101.59.w1)

Paralysis
and death in 3/3 hamsters following intracerebral inoculation and in 2/4 hamsters
following intraperitoneal inoculation. During an outbreak in Israel (Maayan Zvi),
1951. (J100.93.w1)

Experimental infection by intraperitoneal infection. Illness developed by 6-7 days after
inoculation with neurological signs by seven days and death at 7-14 days (in about half
the animals) or recovery but with residual neurological signs. (J84.7.w20,
J91.65S3.w2)

No signs for the first five days after infection. Lethargy and huddling together in
corners at six or seven days, with reduced feeding, drinking and grooming. (J84.7.w20)

Neurological signs at seven to ten days, such as hind limb paralysis, tremors,
difficulty in walking, loss of balance. (J84.7.w20)

Death of severely affected animals at seven to fourteen days.(J84.7.w20)

No
clinical signs or only a one-day rise in body temperature reported with clinical
infection; seroconversion occurs with development of a high titre of antibodies. (J100.93.w1,
J101.59.w1,
J120.20.w1,
J122.77.w1)

No
clinical signs following very high dose intracerebral inoculation. Seroconversion occurs.
(J101.59.w1)

No
clinical signs following intracerebral inoculation of two adults and only very slight
local reaction with intracorneal inoculation. Development of neutralizing antibodies by 19
days after inoculation in 1/1 of each set of rabbits (only one of each set tested).
(J120.20.w1)

One-day rise in body temperature in some individuals, otherwise no clinical signs
following intracerebral inoculation. Circulating virus demonstrated (by mouse inoculation)
on the first and second days post-inoculation. During an outbreak in Israel (Maayan Zvi),
1951. (J100.93.w1)

No clinical signs following intracerebral inoculation but development of high titre
antibodies. No clinical signs in response to inoculation onto scarified cornea. Egypt
strain, 1950. (J122.77.w1)

Usually asymptomatic but may result in illness involving non-specific
signs such as depression, anorexia, weakness, weight loss and recumbency, or neurological
signs which may include abnormal posture of the head or neck, ataxia, tremors, circling,
disorientation posterior paresis (unilateral or bilateral) and visual impairment. Sudden
death may also occur.

Clinical illness may result in recovery (usually following mild clinical
signs) or death after a period of 1-24 days, although clinical illness most commonly has
been reported to last less than one week.

Duration and titre of viraemia varies between species, as shown by
experimental infection.

"The clinical signs of WNV infection in WCS [Wildlife
Conservation Society] collection birds were usually nonspecific. Some were found
dead with no premonitory signs. Many exhibited depression, anorexia, weakness, weight
loss, and recumbency. However, several birds had neurological abnormalities including
abnormal head or neck posture, ataxia, tremors, circling, disorientation, unilateral or
bilateral posterior paresis, and impaired vision. The course of clinical illness was
usually less than one wk, but ranged from 1-24 days before recovery or death.
Hematological and biochemical changes were variable and nonspecific." (P30.1.w3)

Pathological
examination of 27 birds of 14 species in eight orders that were naturally infected with WN
virus in a New York City zoological collection in 1999 revealed a variety of lesions. The
most prominent lesions were gross brain haemorrhage, splenomegaly, meningoencephalitis and
myocarditis. Virus was isolated from the
kidney, (20/20 birds), heart (4/25), intestines, (13/14), brain (23/26), spleen (15/18),
pancreas (10/12), adrenal, (10/13), liver (14/20), ovaries (4/8) and lungs (5/12 birds) (J26.37.w1).

Twelve
species of wild birds in the United States became viremic following experimental infection
with the 1999 New York strain of WN virus, but titers varied greatly among the species.
(J91.65S3.w1)

Commonly a fatal infection in crows. Clinical signs which may be seen include general
signs of weakness and lethargy, standing with a crouched posture and with difficulty in
maintaining balance, inability to walk, perch, stand, fly or to hold the wings in their
normal position against the body and lack of a normal response to danger. Prostration and
convulsions may be seen prior to death. (V.w42)

Severe clinical disease with high morbidity and mortality has been seen in naturally
affected young geese (3-8 weeks old) in Israel. In Hungary, fatal
infection with neurological signs was seen in 6-10 week old geese. Experimental subcutaneous infection of
four two-week-old goslings resulted in decreased activity, depression and weight loss,
with death of two birds and nervous signs (intermittent torticollis and opisthotonus,
rhythmic side-to-side movement of the head) requiring euthanasia of a third.
(J6.34.w1,
J84.7.w29,
J133.951.w26)

LITERATURE REPORTS:

Experimental subcutaneous inoculation of two-week-old goslings resulted in decreased
activity (4/4); depression (4/4), weight loss (4/4), nervous signs in 1/4: intermittent
torticollis and opisthotonus, rhythmic side-to-side movement of the head. Of the four
geese 2/4 died at five and six days after subcutaneous inoculation while one waseuthanised
ten days after inoculation due to persistent neurological signs. (J84.7.w29)

Natural infection in domestic goose flocks was seen in birds three to eight weeks old.
Morbidity and mortality in affected flocks were severe; clinically affected individuals
presented with paralytic signs. (J133.951.w26)

Fatal infection with neurological signs in a
flock of commercially-reared geese. All geese showing clinical signs
died, at ages 6 -12 weeks, after 4-5 days of clinical signs including
ataxia, incoordination, intermittent torticollis and opisthotonus,
abnormal head position, rhythmic side-to-side head movement, neck
wriggling, and paralysis. It was considered that the coinfection with
circovirus may have made the geese more susceptible to WNV, due to
immunosuppression. (J6.34.w1)

Experimental subcutaneous inoculation of three-week-old turkey poults did not cause any
clinical signs of disease. One turkey died abruptly at eight days post-inoculation,
possibly from peracute bacterial septicaemia; the role of West Nile virus was unclear.
Viraemia was detectable at two to ten days post-inoculation but on average at levels too
low to infect mosquitoes. Seroconversion occurred at seven days post-inoculation. Low
levels of virus shed in faeces were not sufficient to infect in-contact birds. (J5.44.w2)

There are no reports of clinical signs related to natural infection in chickens, nor
have such signs been seen in experimentally infected individuals, even in young chicks.
However infection of young chicks and sometimes of older birds produces viraemia
sufficient to infect mosquitoes, and may also result in cloacal shedding of virus. One
case of apparent transmission from an inoculated bird to its uninoculated control
cage mate
has been recorded. Antibodies may be detected by as soon as five to seven days
post-inoculation, depending on the test used. Inoculation of embryonated hens' eggs
results in lethal infection. (J5.44.w1,
J84.7.w22,
J91.5.w1,
J100.93.w1,
J101.59.w1,
J116.5.w1,
B241.49.w49)

LITERATURE REPORTS:

Experimental infection in young chicks resulted in circulating virus in
titres adequate to infect mosquitoes; in older birds titres sufficient to infect
mosquitoes developed sometimes. (J91.5.w1)

Experimental subcutaneous inoculation of seven-week-old chickens resulted in no clinical
disease, although histopathological lesions could be detected in tissues. Detectable
viraemia occurred at 2-8 days post-infection (DPI), peaking at 105/ml at four
DPI. Antibodies were first detectable at five DPI (PRNT) or seven DPI (IFA, using IgG
conjugate). Virus was isolated from cloacal swabs on days four and five DPI. No
transmission to in-contact chickens occurred. (P32.1.w12,
J5.44.w1)

No clinical signs following subcutaneous inoculation. During an outbreak in Israel
(Maayan Zvi), 1951. (J100.93.w1)

No clinical signs following experimental subcutaneous or mosquito inoculation with
strain WNV-NY99. Development of neutralising antibodies from as early as seven days
post-inoculation and detectable viraemia in 20/21. Cloacal shedding of virus at days 2-6
post-inoculation in some birds (5/5 needle-inoculated, 5/5 60-week-old mosquito-inoculated
and 2/11 17-week-old mosquito-inoculated birds) and virus detected on throat swabs in 2/6
17-week-old birds. One apparent transmission from a needle-inoculated bird to its cage
mate (as shown by a transient low-level viraemia). No development of antibodies or
viraemia following oral inoculation. (J84.7.w22)

Chick embryo:

Yolk sac inoculation resulting in death in 100% of embryos, incubation period 2-3 days.
WN virus strain isolated from a rook (Corvus
frugilegus - Rook) in the Ukraine, 1980. (J116.5.w1)

Yolk
sac or chorioallantoic membrane inoculation resulted in the death of 100% of embryos. (J101.59.w1)

Lethal
infection occurs in embryonated hens' eggs but these are less susceptible than are mice.
(B241.49.w49)

In a wild-born
fledgling Accipiter gentilis - Goshawk being reared at a
temporary rehabilitation facility in Hungary in August 2004, sudden
onset fatal neurological disease including ataxia and head tremors;
terminally, seizures. Milder disease in
its nest mate two weeks later, lasting for a week before recovery. In August 2005, two sick free-ranging
goshawk fledglings were brought to the same centre and were euthanased
with severe neurological signs. Clinical signs also developed in a
juvenile and an adult goshawk on the premises, starting after the sick
goshawks had been euthanised; these two birds were treated
supportively, including force-feeding, and survived; in the adult, the
signs lasted only two days. Rapid loss of body condition during the
illness. (J279.7.w2)

In wild goshawks in Austria, "deviant behaviour caused by
neurological symptoms" followed by sudden death. (J238.149.w1)

Clinical illness has been reported, with an affected bird showing
depression, ataxia and mild seizures. Rapid loss of body condition
during the illness. Recovery following supportive care including
force-feeding. (J279.7.w2)

LITERATURE REPORTS:

In a
fledgling Accipiter nisus - Eurasian sparrowhawk, in 2005,
depression, ataxia and mild seizures. Rapid loss of body condition
during the illness. Recovery following supportive care including
force-feeding. (J279.7.w2)

Spain, 2007. A two-year-old captive bred eagle was found
moribund one month after release into the wild; it was debilitated
and aggressive, became increasingly disorientated, developed a head
tilt and after five days of supportive care, died. An adult male in
a captive pair became disorientated with impaired vision and
debility; he survived after intensive care. (J84.14.w5)

Usually no clinical signs of illness, but clinical illness
(neurological signs) has been reported occasionally crane, in one
crane leading to euthanasia, and weight loss in experimentally
challenged cranes. (J2.40.w3, J4.224.w1,
P87.10.w3)

Progressive ataxia in one elderly (37 years) Florida sandhill
crane which was also quiet and unusually non-aggressive. Developing
from difficulty in balancing to a need to use a wall or its wings to
support itself, with inability to stand unassisted and several
falls, later intention tremor of the head and neck and
proprioceptive deficits in the wings. (P87.10.w3)

General signs of weakness, depression and recumbency and various
neurological signs including incoordination, torticollis and
seizures. (J5.47.w2)

LITERATURE REPORTS:

Observed clinical signs included "weakness, uncoordinated
flight, inability to fly, depression, recumbency, head tilt,
torticollis, tremors, and seizures; three owls were found dead with
no observed signs" (J5.47.w2)